scholarly journals 4-Hydroxynonenal induces apoptosis in human osteoarthritic chondrocytes: the protective role of glutathione-S-transferase

2008 ◽  
Vol 10 (5) ◽  
pp. R107 ◽  
Author(s):  
France Vaillancourt ◽  
Hassan Fahmi ◽  
Qin Shi ◽  
Patrick Lavigne ◽  
Pierre Ranger ◽  
...  
Keyword(s):  
Protective Role ◽  
Glutathione S Transferase ◽  
Osteoarthritic Chondrocytes

scholarly journals Ameliorative Effects of Honey, Propolis, Pollen, and Royal Jelly Mixture against Chronic Toxicity of Sumithion Insecticide in White Albino Rats

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2633 ◽  
Author(s):  
Atef M.K. Nassar ◽  
Yehia M.M. Salim ◽  
Khalid S.A. Eid ◽  
Hazem M. Shaheen ◽  
Abdullah A. Saati ◽  
...  
Keyword(s):  
Royal Jelly ◽  
Corn Oil ◽  
Ethylenediaminetetraacetic Acid ◽  
Reproductive Organs ◽  
Protective Role ◽  
Albino Rats ◽  
Total Protein Content ◽  
Glutathione S Transferase ◽  
Significant Toxicity

Sumithion (Fenitrothion) (SUM) is an organophosphorus insecticide used to combat a wide variety of plant pests. Exposure to SUM causes significant toxicity to the brain, liver, kidney, and reproductive organs through, for example, binding to DNA, and it induces DNA damage, which ends with oxidative stress. Therefore, the present study aimed to examine the protective role of bee products: a mixture of honey, propolis, palm pollen, and royal jelly (HPPJ) against SUM-induced toxicity. Twenty-four male albino rats (Rattus norvegicus) were classified into four groups, each containing six rats: control (corn oil), SUM (85 mg/kg; 1/20 LD50), HPPJ, and SUM + HPPJ once daily for 28 consecutive days. Blood samples were gently collected in sterilized ethylenediaminetetraacetic acid (EDTA) tubes for blood picture analyses and tubes without anticoagulant for serum isolation. Serum was used for assays of enzymatic and biochemical characteristics. The results revealed that SUM increased the weights of the liver, kidney, and brain as well as the enzymatic activity of glutathione peroxidase (GP), serum superoxide dismutase (SOD), and glutathione-S-transferase (GST). Additionally, SUM significantly increased the activity of lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and γ-glutamyltransferase (γ-GT) and glucose, uric acid, and creatinine contents, while decreasing the acetylcholine esterase (AChE) activity and total lipids and total protein content. Furthermore, because of the inclusion of phenolic, flavonoids, terpenoids, and sugars, the HPPJ mixture counteracted the hematological, renal, and hepatic toxicity of SUM exposure.

scholarly journals Protective Effect of Quercetin on Melphalan-Induced Oxidative Stress and Impaired Renal and Hepatic Functions in Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Ebenezer Tunde Olayinka ◽  
Ayokanmi Ore ◽  
Olaniyi Solomon Ola ◽  
Oluwatobi Adewumi Adeyemo
Keyword(s):  
Anticancer Agents ◽  
Hepatic Function ◽  
Protective Role ◽  
Glutathione S Transferase ◽  
Drug Induced ◽  
Treatment Groups ◽  
Plasma Bilirubin ◽  
Male Wistar Rats ◽  
Mda Content

One major challenge with the use of anticancer agents is the phenomenon of drug-induced toxicity. Melphalan (MPLN) is an alkylating anticancer agent, while quercetin (QCT) is an antioxidant. We investigated the protective role of quercetin against MPLN-induced toxicity. Twenty-five male Wistar rats (160–170 g) were randomized into five treatment groups; (I) control, (II) MPLN (0.2 mg/kg b.w.), (III) pre-treated with QCT (20 mg/kg b.w.) for 7 days followed by MPLN (0.2 mg/kg b.w.) for 7 days, (IV) cotreated with QCT (20 mg/kg b.w.) and MPLN (0.2 mg/kg b.w.) for 7 days, and (V) QCT (20 mg/kg b.w.) alone. MPLN caused a significant increase in plasma bilirubin, urea, and creatinine by 122.2%, 102.3%, and 188%, respectively (P<0.05). Similarly, plasma ALP, ALT, AST, and γ-GT activities increased significantly by 57.9%, 144.3%, 71.3%, and 307.2%, respectively, relative to control. However, pre or cotreatment with QCT ameliorated the levels of renal and hepatic function indices. Hepatic ascorbic acid and GSH and activities of glutathione-S-transferase, SOD, and catalase decreased significantly by 36.2%, 188%, 46.5%, 34.4%, and 55.2%, respectively, followed by increase in MDA content by 46.5% relative to control. Pre- and cotreatment with QCT reestablished the hepatic antioxidant status and lipid peroxidation. Overall, quercetin protected against MPLN-induced renal and hepatic toxicity in rats.

scholarly journals Amelioration of Isoproterenol-Induced Oxidative Damage in Rat Myocardium byWithania somniferaLeaf Extract

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Md. Ibrahim Khalil ◽  
Istiyak Ahmmed ◽  
Romana Ahmed ◽  
E. M. Tanvir ◽  
Rizwana Afroz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Troponin I ◽  
Protective Role ◽  
Lipid Profiles ◽  
Enzymatic Antioxidants ◽  
Marker Enzymes ◽  
Glutathione S Transferase ◽  
Myocardial Membrane ◽  
Endogenous Antioxidant

We investigated the protective role ofWithania somniferaleaf extract (WSLEt) on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg body weight (b.w.)) administered to rats for two consecutive days caused a significant increase in cardiac troponin I (cTnI) levels and serum lipid profiles, as well as the activities of some marker enzymes. In addition to these diagnostic markers, there were increased levels of lipid peroxidation (LPO) and decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRx), and glutathione-S-transferase (GST)) in the myocardium. However, oral pretreatment (100 mg/kg b.w.) with WSLEt for 4 weeks elicited a significant cardioprotective activity by lowering the levels of cTnI, lipid profiles, and marker enzymes. The levels of LPO products were also significantly decreased. Elevated activities of antioxidant enzymes were also observed in rats pretreated with WSLEt. As further confirmed histopathologically, our findings strongly suggest that the cardioprotective effect of WSLEt on myocardium experiencing ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidant system and an inhibition of LPO in the myocardial membrane. We conclude that WSLEt confers some protection against oxidative damage in ISO-induced MI in rats.

scholarly journals Biochar and Chitosan Regulate Antioxidant Defense and Methylglyoxal Detoxification Systems and Enhance Salt Tolerance in Jute (Corchorus olitorius L.)

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2017
Author(s):  
Mirza Hasanuzzaman ◽  
Md. Rakib Hossain Raihan ◽  
Ebtihal Khojah ◽  
Bassem N. Samra ◽  
Masayuki Fujita ◽  
...  
Keyword(s):  
Salt Stress ◽  
Biomass Accumulation ◽  
Protective Role ◽  
Monodehydroascorbate Reductase ◽  
Antioxidant Systems ◽  
Corchorus Olitorius ◽  
Glutathione S Transferase ◽  
Detoxification Systems ◽  
Catalase Peroxidase

We investigated the role of biochar and chitosan in mitigating salt stress in jute (Corchorus olitorius L. cv. O-9897) by exposing twenty-day-old seedlings to three doses of salt (50, 100, and 150 mM NaCl). Biochar was pre-mixed with the soil at 2.0 g kg−1 soil, and chitosan-100 was applied through irrigation at 100 mg L−1. Exposure to salt stress notably increased lipid peroxidation, hydrogen peroxide content, superoxide radical levels, electrolyte leakage, lipoxygenase activity, and methylglyoxal content, indicating oxidative damage in the jute plants. Consequently, the salt-stressed plants showed reduced growth, biomass accumulation, and disrupted water balance. A profound increase in proline content was observed in response to salt stress. Biochar and chitosan supplementation significantly mitigated the deleterious effects of salt stress in jute by stimulating both non-enzymatic (e.g., ascorbate and glutathione) and enzymatic (e.g., ascorbate peroxidase, dehydroascorbate reductase, monodehydroascorbate reductase, glutathione reductase superoxide dismutase, catalase, peroxidase, glutathione S-transferase, glutathione peroxidase) antioxidant systems and enhancing glyoxalase enzyme activities (glyoxalase I and glyoxalase II) to ameliorate reactive oxygen species damage and methylglyoxal toxicity, respectively. Biochar and chitosan supplementation increased oxidative stress tolerance and improved the growth and physiology of salt-affected jute plants, while also significantly reducing Na+ accumulation and ionic toxicity and decreasing the Na+/K+ ratio. These findings support a protective role of biochar and chitosan against salt-induced damage in jute plants.

Influence of flavonoid extracts from celery on oxidative stress induced by dichlorvos in rats

2011 ◽  
Vol 31 (6) ◽  
pp. 617-625 ◽  
Author(s):  
J Cao ◽  
X Zhang ◽  
Q Wang ◽  
L Jia ◽  
Y Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treated Group ◽  
Protective Role ◽  
Normal Diet ◽  
Intragastric Administration ◽  
Glutathione S Transferase ◽  
Male Wistar Rats ◽  
Mda Content ◽  
Gpx Activity

The present work was to investigate the effects of flavonoid extracts from celery on oxidative stress induced by dichlorvos (DIC) in male Wistar rats maintained on a normal diet. The rats were given DIC through intragastric administration by the dose of 7.2 mg/kg·body weight (bw)/day and additionally added 5% flavonoid extracts to the diet for 4 weeks continuously. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione- S-transferase (GST) and the content of malondialdehyde (MDA) in livers of rats were measured at the end of the experiment. Under the influence of DIC, there were significant decrease in the activities of SOD, CAT and GST and significant increase in GPx activity and MDA content. The results also showed that the activities of SOD, GST and CAT in the DIC-treated group declined significantly when compared with the flavonoid extracts group and the DIC + flavonoid extracts group, respectively. With regard to GPx activity and MDA content, significant increase were showed in the DIC-treated group in comparison to those in the flavonoid extracts group and the DIC + flavonoid extracts group, respectively. The observations presented lead us to conclude the harmful effects of DIC during the exposure and the protective role of flavonoids in minimizing these effects.

scholarly journals Cellular Apoptosis, Mitochondrial Swelling, Permeability and Cytochrome-C Level After (Fe3o4)-Nps Nanoparticles Exposure and Protective Role of Diferuloylmethane in Rats Liver

2020 ◽  
Vol 7 (1) ◽  
pp. 140-154
Author(s):  
Zina Bouteraa ◽  
Rachid Rouabhi ◽  
Fouad Menaceur ◽  
Salim Gasmi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protective Role ◽  
Mitochondrial Swelling ◽  
Male Rats ◽  
Glutathione S Transferase ◽  
Defensive Role ◽  
Cellular Apoptosis ◽  
Cyt C

AbstractDuring recent years the defensive role of diferuloylmethane against oxidative stress and apoptosis has been experimentally documented. Fe3O4-NPs can cause cellular death by inducing oxidative stress. Present study aimed to investigate whether diferuloylmethane could protect rats mitochondria against Fe3O4-NPs intoxication. Twenty adult male rats were randomly chosen and divided into four groups: control; treated with 10 mg/kg/d of Fe3O4-NPs; treated with diferuloylmethane at the dose 20 ml/kg/d; treated with Fe3O4-NPs (10 mg/kg/d) and diferuloylmethane (20 ml/kg/d) respectively for 28 days. The results showed that Fe3O4-NPs increased the Alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid peroxidation, mit-GSH (Glutathione), mit-CAT (Catalase), mit-GST (Glutathione S-transferase) and decreased mit-GPx (Glutathione peroxidase), with increased in mitochondrial swelling and permeability followed by the increasing level of plasmatic Cyt-c. The addition of diferuloylmethane (DFM) to these samples reduces or corrects the amount of the most of biomarkers. These findings have demonstrated that DFM can act as an antioxidant and antiapoptotic factor against damages induced by Fe3O4-NPs.

scholarly journals Dietary quercetin abrogates hepatorenal oxidative damage associated with dichloromethane exposure in rats

2019 ◽  
Author(s):  
Solomon E Owumi ◽  
Olabisi F Danso ◽  
Magdalene E Effiong
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
Gamma Glutamyl Transferase ◽  
Glutathione S Transferase ◽  
Histological Changes ◽  
Chlorinated Solvent ◽  
Household Products ◽  
Liver And Kidney ◽  
Glutamyl Transferase

Exposure to dichloromethane (DCM), a commonly used chlorinated solvent in industrial settings and for the production of many household products, reportedly elicits detrimental effects in animals and humans. The present study investigated the protective role of dietary quercetin on DCM-induced hepatorenal damage in rats. Experimental rats were orally administered with DCM (150 mg/kg) and 30 min later with quercetin at 10, 20 and 40 mg/kg or none for 7 consecutive days. The results indicated that DCM-mediated significant (p<0.05) increases in serum alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase and alkaline phosphatase activities as well as urea and creatinine levels were dose-dependently normalized to the control values in rats co-treated with quercetin. Further, quercetin co-treatment ameliorated DCM-mediated decrease in the hepatic and renal activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase as well as glutathione level in the treated rats. Moreover, quercetin co-treatment markedly reduced lipid peroxidation level and protected against histological changes in liver and kidney of the treated rats. Taken together, quercetin abrogated hepatorenal oxidative damage in DCM-treated rats via improvement of antioxidant status and suppression of oxidative damage.

scholarly journals Protective role of glutathione S-transferase P1 (GSTP1) Val105Val genotype in patients with bronchial asthma

2003 ◽  
Vol 57 (2) ◽  
pp. 213-217 ◽  
Author(s):  
A. Sükrü Aynacioglu ◽  
Muradiye Nacak ◽  
Ayten Filiz ◽  
Erhan Ekinci ◽  
Ivar Roots
Keyword(s):  
Bronchial Asthma ◽  
Protective Role ◽  
Glutathione S Transferase

scholarly journals Human GSTA1-1 reduces c-Jun N-terminal kinase signalling and apoptosis in Caco-2 cells

2006 ◽  
Vol 400 (1) ◽  
pp. 135-141 ◽  
Author(s):  
Laura Romero ◽  
Kimberly Andrews ◽  
Lorraine Ng ◽  
Kelly O'Rourke ◽  
Ann Maslen ◽  
...  
Keyword(s):  
Uv Irradiation ◽  
Protective Role ◽  
Stress Conditions ◽  
Glutathione S Transferase ◽  
Kinase Activation ◽  
Protein Levels ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Jnk Activation

The effect of GSTA1-1 (glutathione S-transferase Alpha 1-1) on JNK (c-Jun N-terminal kinase) activation was investigated in Caco-2 cells in which GSTA1 expression increases with degree of confluency, and in MEF3T3 cells with Tet-Off-inducible GSTA1 expression. Comparison of GSTA1 expression in pre-confluent, confluent and 8-day post-confluent Caco-2 cells revealed progressively increasing mRNA and protein levels at later stages of confluency. Exposure of pre-confluent cells to stress conditions including IL-1β (interleukin-1β), H2O2 or UV irradiation resulted in marked increases in JNK activity as indicated by c-Jun phosphorylation. However, JNK activation was significantly reduced in post-confluent cells exposed to the same stresses. Western-blot analysis of GSTA1-1 protein bound to JNK protein pulled down from cellular extracts showed approx. 4-fold higher GSTA1-1–JNK complex formation in post-confluent cells compared with pre-confluent cells. However, stress conditions did not alter the amount of GSTA1-1 bound to JNK. The role of GSTA1-1 in JNK suppression was more specifically revealed in Tet-Off-inducible MEF3T3-GSTA1-1 cells in which GSTA1 overexpression significantly reduced phosphorylation of c-Jun following exposure to IL-1β, H2O2 and UV irradiation. Finally, the incidence of tumour necrosis factor α/butyrate-induced apoptosis was significantly higher in pre-confluent Caco-2 cells expressing low levels of GSTA1 compared with post-confluent cells. These results indicate that GSTA1 suppresses activation of JNK signalling by a pro-inflammatory cytokine and oxidative stress and suggests a protective role for GSTA1-1 in JNK-associated apoptosis.

Sign in / Sign up

Export Citation Format

Share Document